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Biomedical subjects

J Bachevalier

Publications and source records attributed to J Bachevalier.

71 records · Page 4Linked to original sources
PubMed1982

Thiamine deficiency and cerebrospinal fluid 5-hydroxyindoleacetic acid: a preliminary study.

In three out of five patients with low cerebrospinal fluid thiamine concentrations, the 5-hydroxyindoleacetic acid (5HIAA) values also were low. All patients received thiamine replacement therapy; they underwent a second lumbar puncture after 13, 6, 7, 5 and 45 days of treatment. In all patients blood and cerebrospinal fluid thiamine values rose after treatment. In those patients with initially low CSF 5HIAA, thiamine treatment increased 5HIAA markedly.

Adult↗
PubMed1981

The blood-brain barrier and folate deficiency.

Twenty-three patients (average age: 63.2 +/- 14.9 (x +/- SEM) ranging from 28 to 83 yr) with low or borderline cerebrospinal fluid (CSF) folate and low serum underwent two lumbar punctures, i.e., before and after 3 wk of folate therapy. The rise in CSF folate content in the whole group after the replacement therapy was significant by both the Lactobacillus casei and radioisotope methods of folate determination. In patients with folate-responsive neurological disorders, the rise of CSF values after replacement therapy was definitely higher than in the group of patients in whom folate deficiency was not related to the actual clinical picture. Contrary to previous statements, the present study revealed that there is not an absolute blood-brain barrier for folate because the lower the CSF folate level was, the more rapid and spectacular the increase in CSF folate after replacement therapy was found.

Adult↗
PubMed1981

Folic acid absorption test in various clinical conditions.

The folic acid absorption test (FAAT) has carried out in 18 normal control subjects; 8 patients with proven atrophy of the jejunal mucosa; 7 patients with gastric ulcus; 17 patients with reactive hypoglycemia; 13 patients with diabetes mellitus, and, finally, 9 epileptic patients treated with diphenylhydantoin (DPH). The most striking fact in this study is the difference between the FAAT in normal subjects versus patients with atrophy of the jejunal mucosa, reactive hypoglycemia and DPH consumption. On the other hand there were no significant differences in folate absorption between controls and diabetic patients.

Adult↗
PubMed1981

Blood thiamine and blood folate levels. A comparative study in control, alcoholic and folate-deficient subjects.

A group of 85 patients underwent serum, red blood cell (RBC) folate and whole blood thiamine determinations. The group was divided into three subgroups: 1) a control group (41 patients who had no neurological or mental disorders which could be attributable to a vitamin deficiency); 2) a subgroup of folate-deficient patients (29 Ss) who had folate-responsive neuropsychiatric symptoms and 3) 15 alcoholic patients. There was no significant correlation between blood thiamine levels on one hand and serum and RBC folate on the other in the entire group. Alcoholic patients showed significant lower whole blood thiamine levels (p less than .001) and lower RBC folate (p less than .025) as compared with controls. We conclude that in the great majority of folate-deficient patients there is no correlation between folate and thiamine blood levels.

Adolescent↗
PubMed1980

Acquisition and retention of classical conditioning in the newborn rat.

The development of memory of a conditioned response was examined in London black rats between 0 and 4 days of age. For the conditioning, a vibrotactile stimulus paired with an electric shock was presented to the animal 80 times with an interval of 2000 msec between stimuli. The animals were retested at retention intervals of 3 min or 24 hr. The results showed that 0-, 2-, 3-, and 4-day-old rats possess a retention capacity of at least 24 hr and suggest that the emergence of memory may be task-specific.

Animals↗
PubMed1980

Dietary folic acid and the activity of brain cholinergic and gamma-aminobutyric acid (GABA) enzymes.

Charles River CD male rats were randomly divided into 3 groups of five each and placed on folate deficient, folate excess, and control diets respectively. glutamate decarboxylase GAD gamma-amino-butyrate aminotransferase (GABA-T), choline acetltransferase (ChAc), and acetylcholinesterase (AChE) were assayed in the rat brains after 6 weeks of dietary treatment. Neither folate deficiency nor folate supplementation influenced the enzymes associated with GABA and acetylcholine metabolism.

Acetylcholinesterase↗
PubMed1978

Polyneuropathy and folate deficiency.

We studied five patients (two men and three women, age between 58 and 76 years) with clinical and electrophysiological signs of polyneuropathy. Routine neurological, hematological, and gastroenterological studies as well as procedures to test fat malabsorption were performed. Folate determinations were done using both radioactive and Lactobacillus casei methods. Two patients displayed the signs of subacute combined degeneration of the spinal cord with polyneuropathy, while three had only signs of neuropathy. All had low serum folate concentration, long-standing gastrointestinal disease, and deficient folate intake. The D-xylose absorption test gave values in all patients, while none displayed the classical malabsorption syndrome. The patients had substantial improvement or recovered (according to clinical and electrophysiological measurements) after periods ranging from 9 to 39 months of folate therapy. Such acquired folate-responsive polyneuropathy has two principal characteristics: mixed sensorimotor with mainly sensory deficits, and involvement of one or both of the lower extremities much more extensively than the upper extremities.

Aged↗
PubMed1978

Avoidance behavior in folate--deficient rats.

The effects of folate deficiency in post-weanling male rats in an active avoidance learning test were studied. Ingestion of a folate-free diet for 3 weeks markedly decreased serum and erythrocyte folate concentrations but had only a slight effect on growth rate. The decrease in blood folates was correlated with an increase in the number of trials necessary to reach criterion in the learning test. There was no motor impairment since the mean escape latency was the same in control and folate-deficient animals. These results suggest that folic acid deficiency started at weaning could be responsible for learning impairment.

Animals↗
PubMed1977

Folate-responsive neurological and mental disorders: report of 16 cases. Neuropsychological correlates of computerized transaxial tomography and radionuclide cisternography in folic acid deficiencies.

Two groups of patients with folic acid responsive neurological and psychiatric disorders are reported. The first group (7 patients) had well-established acquired folate deficiency due either to defective absorption (4 cases with atrophy of jejunal mucosa) or to a deficient diet (3 cases). One patient had a subacute combined degeneration of the spinal cord while others were depressed and had weight loss, permanent muscular and intellectual fatigue, restless legs syndrome, depressed ankle jerks, diminution of the sense of vibration in the knees and a stocking-type tactile hypoesthesia. The second group (9 patients) comprised idiopathic cases of folic acid deficiency. Their main subjective complaints were chronic fatigability and familial restless legs syndrome. The neurological findings were similar to those of the patients with acquired disorders. Neuropsychological testing procedures revealed an abnormal intellectual functioning in all 16 patients. Abnormal patterns of radionuclide cisternograms and computerized transaxial tomography (CTT) were found in 11 patients. After 6-12 months of folic acid therapy a striking improvement regarding their intellectual functioning was noticed: the IQ, Kohs Block Design and Category tests were significantly improved. The correlation of neuropsychological findings with CTT and radionuclide cisternograms led to the conclusion that chronic folate deficiency could induce cerebral atrophy.

Adult↗
PubMed1975

Effect of atropine on behavioral arousal in the developing rat.

Atropine-induced changes in behavioral arousal were examined in the developing rat between 21 and 40 days of age using a single exploratory trial on an elevated T-maze. Under atropine (10 mg/kg, i.p.) spontaneous activity as measured by numbers of errors, rearing responses, and stereotyped responses was significantly decreased in animals less than 25 days of age. It was significantly increased, however, between 26 and 30 days, with maximal action on the 28th day. After 30 days the effect of atropine was negligible. These results support the hypothesis of a cholinergic inhibitory mechanism controlling behavioral arousal and becoming efficient after the 25th day of life.

Aging↗
PubMedDate not supplied

Age differences in recognition memory of the rhesus monkey (Macaca mulatta).

Aging is accompanied by a gradual decline in memory in both humans and nonhuman primates. To determine whether the impairment in nonhuman primates extends to recognition memory, which is a sensitive index of the integrity of the limbic system, we trained rhesus monkeys of four different age groups (3-6, 14-17, 20-24, and 25-29 years of age) on a delayed nonmatching-to-sample task with trial-unique objects. After the animals had learned the task, which required recognition of single objects presented ten seconds earlier, memory demands were increased by gradually lengthening delay intervals (to 120 seconds) and list lengths (to ten objects). With increasing age, only marginal impairments in learning the basic task were observed. However, clear age-related differences did emerge when either delays or list lengths were increased, with the oldest group of monkeys demonstrating the greatest impairments. The decline in visual recognition ability in aging monkeys parallels the decline in memory observed with advancing age in humans.

Aging↗
PubMedDate not supplied

Aged monkeys exhibit behavioral deficits indicative of widespread cerebral dysfunction.

To determine whether the decline of behavioral abilities with aging in monkeys is selective or widespread, we examined 18 monkeys ranging from 3 to 34 years of age on a wide variety of tests with the ultimate goal of correlating behavioral deficits with age-related changes in the brain. In our initial study we found impaired visual recognition ability in the aged monkeys (43). In the present study, we assessed the same animals on tests of spatial memory, visual habit formation, visuospatial orientation, visually guided reaching, motor skill learning, and reaction time, these categories having been chosen to test the integrity of different cerebral systems. There were three major findings. First, age-related impairments were observed in nearly all test categories, though often not on easy versions of the tests, suggesting that the deficits observed were in the specific abilities measured and not an artifact of lowered motivation or other general disability. Second, the behavioral decline began in the late teens for certain spatial abilities but did not affect other abilities until the late 20's, suggesting that although the cerebral dysfunction eventually becomes widespread, the cerebral systems underlying spatial abilities are compromised by aging earlier than others. Finally, the finding of correlations between scores of aged animals primarily within test categories as opposed to across categories suggests that different animals have different patterns of cerebral involvement.

Aging↗
PubMedDate not supplied

Connections of inferior temporal areas TEO and TE with parietal and frontal cortex in macaque monkeys.

Inferior temporal cortex is perhaps the highest visual processing area and much anatomical work has focused on its connections with other visual areas in temporal and occipital cortex. Here we report connections of inferior temporal cortex with regions in the frontal and parietal lobes. Inferior temporal areas TEO and TE were injected with WGA-HRP and 3H-AA, respectively, or vice versa, in 1-week-old infant and 3-4-year-old adult monkeys (Macaca mulatta). The results indicated that whereas TEO has more extensive connections with parietal areas, TE has more extensive connections with prefrontal areas. Thus, in the intraparietal sulcus, area TEO is connected with areas LIPd, LIPv, and V3A, and with the as yet undefined region between LIPv and V3A, whereas the connections of TE are predominantly with LIPd, and to a lesser extent with LIPv. In the prefrontal cortex, area TE is connected with areas 8 and 45 in the inferior limb of the anterior bank of the arcuate sulcus, with area 12 on the inferior prefrontal convexity, and with areas 11 and 13 on the orbital surface. By contrast, the connections of area TEO are limited to areas 8, 45, and 12. Furthermore, within prefrontal cortex, the projections from areas TEO and TE terminate in different layers in areas 8 and 45, such that those from TEO terminate in all layers, whereas those from TEO terminate in layers I and V/VI only. In contrast to the connections of areas TEO and TE with various medial temporal-lobe and subcortical structures, which are immature in infant monkeys (Webster et al., 1991, 1993b), the connections with parietal and prefrontal areas appear adult-like as early as 1 week of age.

Aging↗
PubMedDate not supplied

Functional development of the corticocortical pathway for motion analysis in the macaque monkey: a 14C-2-deoxyglucose study.

The corticocortical pathway for motion analysis transmits visual information from striate cortex (V1) via V2, V3d, superior temporal sulcal areas MT, MST, and FST to motion-sensitive areas in the floor and upper bank of the anterior part of the superior temporal sulcus (AST). We studied the functional development of this pathway by applying the 14C-2-deoxyglucose method to rhesus monkeys (Macaca mulatta) ranging in age from 2 d to 3-4 years. A comparison of local cerebral glucose utilization (LCGU) in an intact and a visually deafferented hemisphere in each animal across the age range revealed that this pathway, immature at birth, reaches adult-like levels at 3 months of age. This developmental time course is reflected both in absolute LCGU and in the interhemispheric LCGU differences in all the areas of the pathway. At all ages, the interhemispheric difference in LCGU is largest in V1 and gradually declines along the pathway until a minimum is reached in AST. This decline likely reflects an increasing proportion of nonvisual inputs to the higher-order areas of the pathway. Measurements like those above taken in areas of inferior parietal cortex indicate that they mature at the same rate as those in the motion analysis pathway. However, comparison with findings on the functional development of the temporal areas of the occipitotemporal pathway for object vision (Bachevalier et al., 1991) suggests that areas along the motion analysis pathway and those in parietal cortex mature about 1 month earlier.

Age Factors↗